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Seyed Ehsan Mousavi, Komeil Razmi, and Jawahar G Patil

Built on our recent work that heart rates and function in G holbrooki are sexually dimorphic, this study assessed whether the species is an appropriate model to study sex-hormone effects on heart physiology. With a hypothesis that 17β-estradiol (E2) and 17α-methyltestosterone (MT) regulate the heart rate of juvenile G. holbrooki in a sex-specific manner, genetic males and females were treated with E2 and MT, respectively and the HR (bpm) was measured an hour following treatment using light-cardiogram. Results showed the HR (bpm) of both sexes were significantly (p < 0.05) altered compared to controls. Specifically, the E2 accelerated HR in the males and conversely MT decelerated the HR in the females. The normal expression levels of estrogen (erα and erβ) and G protein-coupled estrogen (gper) receptor genes were significantly higher (p < 0.05) in female than male hearts. Interestingly, the activity of the erβ in the heart of the MT-treated females reversed and was significantly lower (p < 0.05) than those of males while erα and gper were non-responsive. In contrast, significant down- and up-regulation of erα and gper, respectively occurred in the liver of MT-treated females. Morphological observations suggest that MT caused hepatomegaly, somewhat resembling an inflating balloon, perhaps induced by the accumulation of unexpelled gases. While E2 induced ventricular angiogenesis in males was likely due to an influx of blood supply caused by the increased heart rates. Collectively, the results demonstrate that the juvenile G. holbrooki heart readily responds to E2/MT in a sex-specific manner.